Neuromuscular complications of critical illness

BACKGROUND- Neuromuscular weakness is common in the setting of critical illness. Over the past two decades, ii has been recognized that polyneuropathy or myopathy may develop de novo as a complication of the underlying illness, sepsis, or the medical therapies. This weakness complicates recovery and often contributes to prolonged ventilator dependence. REVIEW SUMMARY- The neuromuscular complications of critical illness include critical illness polyneuropathy, an acute myopathy, and prolonged pharmacologic neuromuscular blockade. As a complication of critical illness and the systemic inflammatory response syndrome (usually produced by sepsis), an axonal sensory-motor polyneuropathy may be seen. A myopathy, often called acute quadriplegic myopathy, may develop in a similar setting, often in association with the use of corticosteroids and/or nondepolarizing neuromuscular-blocking agents (NMBAs). Weakness in this latter disorder may result from electrical inexcitability of muscle due to altered membrane sodium channels with reduced sodium currents and loss of myosin thick filament. Some patients, particularly those with abnormal renal or hepatic function, may have prolonged weakness for as long as one week after the use of NMBAs. This large, heterogeneous group of patients are difficult to evaluate due to the limitations imposed by the critical care setting and may have critical illness polyneuropathy, acute quadriplegic myopathy, or both. CONCLUSIONS- Neuromuscular weakness may occur in association with a combination of risk factors, including sepsis and multiorgan failure (systemic inflammatory response syndrome), high-dose corticosteroids, and NMBAs. This may take the form of an axonal polyneuropathy, an acute myopathy, or both.